User:Tkadm30/Notebook/chim trills notebook/Research: Difference between revisions
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Epidemiological evidences of PM2.5-mediated damage to '''neuroimmune''' system: | Epidemiological evidences of PM2.5-mediated damage to '''neuroimmune''' system: | ||
* Alteration of cytokines production | * Alteration of cytokines production | ||
* Stress-induced neuroinflammation (GSK3, TLR4)<cite>Paper1</cite> | * Stress-induced neuroinflammation (GSK3, AKT, TLR4)<cite>Paper1</cite> | ||
* Mitochondrial DNA (mtDNA) oxidative stress (Aluminium oxide?) | * Mitochondrial DNA (mtDNA) oxidative stress (Aluminium oxide?) | ||
* Microglial activation markers? (MAC1, Glutaminase, TLR2)<cite>Paper2</cite> | * Microglial activation markers? (MAC1, Glutaminase, TLR2)<cite>Paper2</cite> |
Revision as of 09:57, 18 March 2017
Research topics
Translocation and internalization of metal oxide nanoparticles (PM2.5)
- Aluminium-induced neurotoxicity and chronic neuroinflammation in the microglia
- Translocation of PM2.5 to the brain.
- The Effects of Nanomaterials as Endocrine Disruptors.
Translocation of aluminium oxide nanoparticles in the microglia
Nanotoxicity and genotoxicity of drug nanoparticles exposure
- The immunological nanotoxicity and genotoxicity of fine particulate matter (PM2.5) is under investigation.
- The chemical clumping behavior of PM2.5 nanoparticles may require a ultrasonic atomization delivery system.
- The synthetic nature of PM2.5 require further research.
Characterization of the Gulf War Syndrome/X variant
The phenotype of the Gulf War Syndrome/X variant (GWSX) is not well characterized. The immunotoxicity and nanotoxicity of PM2.5 nanoparticles require further research.
Epidemiological evidences of PM2.5-mediated damage to neuroimmune system:
- Alteration of cytokines production
- Stress-induced neuroinflammation (GSK3, AKT, TLR4)[1]
- Mitochondrial DNA (mtDNA) oxidative stress (Aluminium oxide?)
- Microglial activation markers? (MAC1, Glutaminase, TLR2)[2]
- Decrease in neurotrophin expression
- Modulation of neuroendocrine response
- Alteration of miRNA expression (miR-15, miR-146a, miR-222)
- Autoimmune limbic encephalitis [3]
Nanotoxicity of metal oxides nanoparticles:
- Aluminium oxide nanoparticles may induce proinflammatory response and oxidative stress.
See also:
- The neuroendocrinology of chronic fatigue syndrome.
- Aluminium oxide nanoparticles induce mitochondrial-mediated oxidative stress and alter the expression of antioxidant enzymes in human mesenchymal stem cells.
- Limbic encephalitis
- Topic: Neurovascular and neuroinflammation mechanisms associated with bipolar disorder
Nanoparticle-based drug delivery
Translocation and internalization of NPs:
- Synthetic nucleic acid delivery systems
- Engineered nanoparticles can be developed to enter blood-brain barrier through intracellular (siRNA) delivery.
- Cellular internalization of quantum dots.
Aerosolized drug nanoparticles
- Photoactivated drug delivery vectors
- Monodisperse aerosols
Research projects
Differential effects of drug nanoparticles on the neuroimmune system and microglial cells
I aim to understand the nanotoxicity and genotoxicity of long-term PM2.5 exposure on physiological and neurological processes:
- In summary, I'm interested to understand the effects of PM2.5 nanoparticles on chronic pulmonary diseases (COPD), miRNA expression (synaptic plasticity) and TLR signaling.
- The differential effects of drug nanoparticles on chronic neuroinflammation and microglial activation (reactive microgliosis) require further research.
Keywords: metal oxides, nanoparticles, bioaerosol, drug delivery, CNS, neuroinflammation, microglia, PM2.5, TLR-2
Knowledge is power: Psychology of modern psychochemical warfare.
Clandestine geoengineering activity is a controversial issue. The aim of this research project is to understand how artificial intelligence is used to deter scientific research on PM2.5.
Keywords: psychology, consciousness, psychochemicals, science, deception, media blackout, cognitive dissonance, disinformation, cognitive infiltration, education, research, PM2.5
References
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Stress-induced neuroinflammation is mediated by GSK3-dependent TLR4 signaling that promotes susceptibility to depression-like behavior
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Involvement of TLR2 and TLR4 in inflammatory immune responses induced by fine and coarse ambient air particulate matter.
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Autoimmune limbic encephalitis presenting as relapsing psychosis